These data are in agreement with global proteomics analysis of UFSP1−/−, UFSP2−/−, and UFSP1/2−/− cell lines that support a hitherto unappreciated role for protein UFMylation in tissue homeostasis thereby explaining UFM1 involvement in SEMD [13]. The gene discussed is UFM1; the disease is spondyloepimetaphyseal dysplasia.